1. Terson Syndrome: a prospective analysis of 45 consecutive patients
George Hadjigeorgiou
Department of Neurosurgery
Red Cross Hospital
Athens, Greece

2. Introduction
First described in 1900 by Albert Terson, as the presence of vitreous hemorrhage in patients with SAH

3. Introduction
Castren, 1963: modification in order to include other forms of intraocular hemorrhage (retinal, subhyaloid)
Manschot, 1944: associated TS with increased mortality

4. Material & Methods Prospective, non-randomized case series study
45 consecutive patients, who were admitted to our clinic with the diagnosis of aneurysmal SAH
All patients underwent a 4-vessel DSA
Indirect opthalmoscopy under mydriasis was performed in all patients upon admission and on the 7th day
Exclusion criteria: causes of SAH other than aneurysmal rupture (e.g. AVM), death of the patient before the opthalmological examination, traumatic SAH
Classification according to the GCS, Hunt&Hess and Fischer grade on admission and according to GOS on discharge

5. Results 45 pt with aSAH: 14 males (31%), 31 females (69%)
Mean age 52.1 yo
Endovascular treatment 37 pt – clipping 8 pt
TS in 6/45 pt (13,3%)  2 males , 4 females
All cases of TS-group were related to aneurysms localized in the anterior circulation

6. Results GCS w/o TS TS 15 16 12-14 11 9-11 6 1 6-8 2 3 3-5 4 H & H
12-14 11
9-11 6 1
6-8 2 3
3-5 4
H & H
w/o TS TS I 5 II 12
III 16 1 IV 4 V 2
Fisher
w/o TS TS I 1 II 15
III 18 5 IV

7. Results
GOS
Pt w/o TS
Pt with TS 1 6 2 4 3 12 10 5 7

8. Discussion TS is a common phenomenon
Studies have estimated that 12-16% of patients with SAH do not reach hospital to be clinically assessed (Pobereskin, 2001)
Prospective Study
No of Patients with SAH
% with TS
Garfinkle et al (1992) 22
27 %
Pfausler et al (1996) 60
17%
Frizzeli et al (1997) 99 8%
Fountas et al (2008)
174
12,1%
He et al (2011)
101
14,8%
Watanabe et al (2011) 47
29%
Stienen et al (2012)
18,3%
Current Study 45
13,3%

9. Discussion Pathogenesis of TS proposed mechanisms:
Increased ICP may force blood into the subarachnoid space and along the optic nerve sheath into the preretinal space (Muller, 1974)
Compression of the central retinal vein and retinochoroidal anastomoses by elevated CSF pressure causing venous hypertension and disruption of retinal veins (Garfinkle, 1992)

10. Discussion
A higher frequency of TS was demonstrated in patients with low GCS, high H&H and Fisher grade
TS-group displayed a significantly worse outcome (GOS: 1,8 vs 3,2) and a higher mortality rate than the non-TS group (33,3% vs 15,4%)
All patients with TS in our study had conservative treatment for the ocular hemorrhage; however it is described that in some cases opthalmic surgery (eg. vitrectomy) may be required (Garweg, 2009)

11. Discussion
In our study, all the cases of the TS-group were related to aneurysms localized in the anterior circulation
However, neither our study nor previous ones in the literature could find a statistical significance correlation between the aneurysm localization and incidence of TS

12. Discussion
For the diagnosis of TS a precise fundoscopy remains the most sensitive method
Fundoscopy may be limited in an acutely ill patient; need for pupil’s size examination
CT: may identify up to 66,7% of TS cases  thickening, nodularity or crescent-shaped increased density of the retinal surface (Swallow, 1998)
Ocular U/S: confirm diagnosis and detection of secondary complications (eg. retinal detachment)

13. Conclusions
TS is a relatively common phenomenon in patients with SAH and is an underdiagnosed complication in the daily hospital routine
TS is an indicator of poor prognosis
An early recognition of TS is important since a permanent impairment of vision may occur
For the accurate assessment of TS and whether intraocular hemorrhage is an independent prognostic variable in patients with SAH, larger and ideally population based prospective studies are required

14. Thank you!